Burn injury is accompanied by marked change in host defense mechanisms. Further consequences of thermal injury are anemia, sepsis, increased metabolic rate and malnutrition. Successful host defense and repair after thermal injury is, in part, dependent on the presence of adequate numbers of highly motile lymphomyeloid cells such as granulocytes, macrophages and monocytes. We propose to systematically analyze the effects of burn injury as well as supervening events such as anemia, sepsis and malnutrition on lymphomyelopoiesis and on the distribution of granulocytes, monocytes and macrophages. We plan to use a model of full-thickness burn injury in mice. Using in vivo and in vitro clonal cultures of myeloid stem cells and progenitor cells, lymphomyelopoiesis will be analyzed after thermal injury, anemia, sepsis and/or malnutrition. The distribution of granulocytes, monocytes and macrophages in the extra lymphomyeloid compartments will be assayed. After initial characterization of the model, further studies are planned to assess the effects of therapy including antimicrobial agents and biologic response modifiers.